<p>Despite consistent links between personality traits and poor sleep, little is known about genetic and environmental influences that may produce them. This study examined how much genetic background and environmental experiences contributed to phenotypic linkages between personality and subjective sleep quality. Seven hundred and thirty-four twin pairs from the Minnesota Study of Twin Aging and Development rated their sleep quality and provided personality reports. Bi-variate analyses revealed that genetic factors accounted for the majority of observed associations between subjective sleep quality and most traits, but also that non-shared environmental experience also played a role that varied across traits. The findings strongly implicate genotype in tying subjective sleep quality to personality variation, alongside non-shared environmental influences, indicate influences unique to individual traits.</p>

Genetic factors explain a major proportion of human height variation, but differences in mean stature have also been found between socio-economic categories suggesting a possible effect of environment. By utilizing a classical twin design which allows decomposing the variation of height into genetic and environmental components, we tested the hypothesis that environmental variation in height is greater in offspring of lower educated parents. Twin data from 29 cohorts including 65,978 complete twin pairs with information on height at ages 1 to 69 years and on parental education were pooled allowing the analyses at different ages and in three geographic-cultural regions (Europe, North America and Australia, and East Asia). Parental education mostly showed a positive association with offspring height, with significant associations in mid-childhood and from adolescence onwards. In variance decomposition modeling, the genetic and environmental variance components of height did not show a consistent relation to parental education. A random-effects meta-regression analysis of the aggregate-level data showed a trend towards greater shared environmental variation of height in low parental education families. In conclusion, in our very large dataset from twin cohorts around the globe, these results provide only weak evidence for the study hypothesis.

We investigated the heritability of educational attainment and how it differed between birth cohorts and cultural–geographic regions. A classical twin design was applied to pooled data from 28 cohorts representing 16 countries and including 193,518 twins with information on educational attainment at 25 years of age or older. Genetic factors explained the major part of individual differences in educational attainment (heritability: a2 = 0.43; 0.41–0.44), but also environmental variation shared by co-twins was substantial (c2 = 0.31; 0.30–0.33). The proportions of educational variation explained by genetic and shared environmental factors did not differ between Europe, North America and Australia, and East Asia. When restricted to twins 30 years or older to confirm finalized education, the heritability was higher in the older cohorts born in 1900–1949 (a2 = 0.44; 0.41–0.46) than in the later cohorts born in 1950–1989 (a2 = 0.38; 0.36–0.40), with a corresponding lower influence of common environmental factors (c2 = 0.31; 0.29–0.33 and c2 = 0.34; 0.32–0.36, respectively). In conclusion, both genetic and environmental factors shared by co-twins have an important influence on individual differences in educational attainment. The effect of genetic factors on educational attainment has decreased from the cohorts born before to those born after the 1950s.

Genome-wide association studies (GWASs) are a popular tool for detecting association between genetic variants or single nucleotide polymorphisms (SNPs) and complex traits. Family data introduce complexity due to the non-independence of the family members. Methods for non-independent data are well established, but when the GWAS contains distinct family types, explicit modeling of between-family-type differences in the dependence structure comes at the cost of significantly increased computational burden. The situation is exacerbated with binary traits. In this paper, we perform several simulation studies to compare multiple candidate methods to perform single SNP association analysis with binary traits. We consider generalized estimating equations (GEE), generalized linear mixed models (GLMMs), or generalized least square (GLS) approaches. We study the influence of different working correlation structures for GEE on the GWAS findings and also the performance of different analysis method(s) to conduct a GWAS with binary trait data in families. We discuss the merits of each approach with attention to their applicability in a GWAS. We also compare the performances of the methods on the alcoholism data from the Minnesota Center for Twin and Family Research (MCTFR) study.

The familial resemblance in length of adult life is very modest. Studies of parent-offspring and twins suggest that exceptional health and survival have a stronger genetic component than lifespan generally. To shed light on the underlying mechanisms, we collected information on Danish long-lived siblings (born 1886–1938) from 659 families, their 5379 offspring (born 1917–1982), and 10,398 grandchildren (born 1950–2010) and matched background population controls through the Danish 1916 Census, the Civil Registration System, the National Patient Register, and the Register of Causes of Death. Comparison with the background, population revealed consistently lower occurrence of almost all disease groups and causes of death in the offspring and the grandchildren. The expected incidence of hospitalization for mental and behavioral disorders was reduced by half in the offspring (hazard ratio 0.53, 95% confidence interval 0.45–0.62) and by one-third in the grandchildren (0.69, 0.61–0.78), while the numbers for tobacco-related cancer were 0.60 (0.51–0.70) and 0.71 (0.48–1.05), respectively. Within-family analyses showed a general, as opposed to specific, lowering of disease risk. Early parenthood and divorce were markedly less frequent in the longevity-enriched families, while economic and educational differences were small to moderate. The longevity-enriched families in this study have a general health advantage spanning three generations. The particularly low occurrence of mental and behavioral disorders and tobacco-related cancers together with indicators of family stability and only modest socioeconomic advantage implicate behavior as a key mechanism underlying familial aggregation of exceptional health and survival.

<p>The Interplay of Genes and Environment across Multiple Studies (IGEMS) is a consortium of 18 twin studies from 5 different countries (Sweden, Denmark, Finland, United States, and Australia) established to explore the nature of gene–environment (GE) interplay in functioning across the adult lifespan. Fifteen of the studies are longitudinal, with follow-up as long as 59 years after baseline. The combined data from over 76,000 participants aged 14–103 at intake (including over 10,000 monozygotic and over 17,000 dizygotic twin pairs) support two primary research emphases: (1) investigation of models of GE interplay of early life adversity, and social factors at micro and macro environmental levels and with diverse outcomes, including mortality, physical functioning and psychological functioning; and (2) improved understanding of risk and protective factors for dementia by incorporating unmeasured and measured genetic factors with a wide range of exposures measured in young adulthood, midlife and later life.</p>

<p>The Danish Twin Registry (DTR) was established in the 1950s, when twins born from 1870 to 1910 were ascertained, and has since been extended to include twins from birth cohorts until 2009. The DTR currently comprises of more than 175,000 twins from the 140 birth cohorts. This makes the DTR the oldest nationwide twin register and among the largest in the world. The combination of data from several surveys, including biological samples and repeated measurements on the same individuals, and data from Danish national registers provides a unique resource for a wide range of twin studies. This article provides an updated overview of the data in the DTR: First, we provide a summary of the establishment of the register, the different ascertainment methods and the twins included; then follows an overview of major surveys conducted in the DTR since 1994 and a description of the DTR biobank, including a description of the molecular data created so far; finally, a short description is given of the linkage to Danish national registers at Statistics Denmark and some recent examples of studies using the various data resources in the DTR are highlighted.</p>

<p>Genetically informative research designs are becoming increasingly popular as a way to strengthen causal inference with their ability to control for genetic and shared environmental confounding. Co-twin control (CTC) models, a special case of these designs using twin samples, decompose the overall effect of exposure on outcome into a within- and between-twin-pair term. Ideally, the within-twin-pair term would serve as an estimate of the exposure effect controlling for genetic and shared environmental factors, but it is often confounded by factors not shared within a twin-pair. Previous simulation work has shown that if twins are less similar on an unmeasured confounder than they are on an exposure, the within-twin-pair estimate will be a biased estimate of the exposure effect, even more biased than the individual, unpaired estimate. The current study uses simulation and analytical derivations to show that while incorporating a covariate related to the nonshared confounder in CTC models always reduces bias in the within-pair estimate, it will be less biased than the individual estimate only in a narrow set of circumstances. The best case for bias reduction in the within-pair estimate occurs when the within-twin-pair correlation in exposure is less than the correlation in the confounder and the twin-pair correlation in the covariate is high. Additionally, the form of covariate inclusion is compared between adjustment for only one’s own covariate value and adjustment for the deviation of one’s own value from the covariate twin-pair mean. Results show that adjusting for the deviation from the twin-pair mean results in equal or reduced bias.</p>

<div class="abstract" data-abstract-type="normal"><div class='sec'><span class="bold">Background</span><p>Parental characteristics and practices predict borderline personality disorder (BPD) symptoms in children. However, it is difficult to disentangle whether these effects are genetically or environmentally mediated. The present study examines the contributions of genetic and environmental influences by comparing the effects of familial risk factors (i.e. parental psychopathology and borderline traits, maladaptive parenting, marital discord) on child BPD traits in genetically related (biological) and non-related (adoptive) families.</p></div><div class='sec'><span class="bold">Methods</span><p>Data are from 409 adoptive and 208 biological families who participated in the Siblings Interaction and Behavior Study (SIBS) and 580 twin families the Minnesota Twin Family Study (MTFS). Parent characteristics and practices included parental psychopathology (measured via structured clinical interviews), parental BPD traits, parenting behaviors, and marital discord. A series of multi-level regression models were estimated to examine the relationship of familial risk factors to child BPD traits and to test whether children's adoptive status moderated the association.</p></div><div class='sec'><span class="bold">Results</span><p>Symptom counts of parents' conduct disorder, adult antisocial behavior, nicotine, alcohol, and illicit drug dependence, and paternal BPD traits substantially predicted child BPD traits only in biological offspring, implying genetic transmission. Maternal BPD traits and both maternal and paternal conflict, lack of regard, and lack of involvement predicted offspring BPD traits regardless of the adoptive status, implying environmental transmission.</p></div><div class='sec'><span class="bold">Conclusions</span><p>Parental externalizing psychopathology and father's BPD traits contribute genetic risk for offspring BPD traits, but mothers' BPD traits and parents' poor parenting constitute environmental risks for the development of these offspring traits.</p></div></div>

We first confirmed adolescents diagnosed with disruptive behavior disorders (oppositional defiant, conduct disorder; n = 158) had lower constraint and higher negative emotionality, and greater psychiatric comorbidity and psychosocial dysfunction, relative to adolescents without (n = 755), in a population-based sample enriched for externalizing psychopathology (mean age = 17.90 years; 52% female). We then explored whether different personality types, defined by patterns of personality identified via latent profile analysis, were differently associated with clinical features in adolescents with a disruptive behavior disorder diagnosis. Four distinct personality types (“disinhibited,” “high distress,” “low distress,” “positive”) were meaningfully different from one another. Results highlight personality heterogeneity as a means of identifying individuals at greatest risk for the most deleterious forms of externalizing psychopathology.

Similarities between parent and offspring are widespread in psychology; however, shared genetic variants often confound causal inference for offspring outcomes. A polygenic score (PGS) derived from genome-wide association studies (GWAS) can be used to test for the presence of parental influence that controls for genetic variants shared across generations. We use a PGS for educational attainment (EA3; N ≈ 750 thousand) to predict offspring years of education in a sample of 2517 twins and both parents. We find that within families, the dizygotic twin with the higher PGS is more likely to attain higher education (unstandardized β = 0.32; p < 0.001). Additionally, however, we find an effect of parental genotype on offspring outcome that is independent of the offspring’s own genotype; this raises the variance explained in offspring years of education from 9.3 to 11.1% (∆R2 = 0.018, p < 0.001). Controlling for parental IQ or socioeconomic status substantially attenuated or eliminated this effect of parental genotype. These findings suggest a role of environmental factors affected by heritable characteristics of the parents in fostering offspring years of education.

<p> Prior research has shown that person-level characteristics (e.g., temperament, personality) correlate and interact with social-contextual factors (e.g., parent–child relationship quality, antisocial peer affiliation) to predict adolescent substance use, but less research has examined similar processes for adult substance use problems. We addressed this gap by testing for personality × romantic partner context interplay in relation to symptoms of alcohol use disorder (AUD) at ages 24 and 29. Participants were twins in the longitudinal Minnesota Twin Family Study ( <italic>N</italic> = 2,769; 52% female). Results support the <italic>corresponsive principle of personality</italic> in that we found that key personality traits in late adolescence (low constraint, negative emotionality) predicted subsequent “selection” into key social contexts in early adulthood (poorer quality romantic relationships and greater romantic partner alcohol use), which subsequently reinforced those traits and associated outcomes (including correlated AUD symptoms) through late young adulthood. There were few meaningful gender differences in these associations. There was also no support for the personality × romantic partner context interaction as a significant predictor of AUD symptoms at ages 24 or 29. Taken together with prior studies, these results suggest that such interactions may be less relevant to the development of young adult AUD compared to adolescent substance use problems. </p>

We analyze data from the Minnesota Twin Registry (MTR) and the Socioeconomic Survey of Twins (SST), combined with new mortality data, and contribute to two bodies of literature. First, we demonstrate a beneficial casual effect of education on health and longevity. Literature results on this subject based on natural experiments and twin studies are controversial despite a long history of research. Second, we shed light on how families allocate resources among siblings, another controversial question. We show that if one twin has a poorer health endowment parents will compensate for the difference with more schooling. We argue that we can expect a bias towards detecting a reinforcement case. Despite the bias we still find evidence of compensating behavior. For identification we rely on identical genes in monozygotic twins, gene variation in dizygotic twins, and shared family background in all twins, and control for the key background characteristics of birth weight and disabling injury. We account for measurement error in reported years of schooling.